Federal clinical guidelines for the diagnosis and treatment of iron deficiency anemia in children. Iron deficiency anemia in children

Catad_tema Iron deficiency anemia - articles

Folate deficiency anemia in children

ICD 10: D52

Year of approval (revision frequency): 2016 (review every 5 years)

ID: KR540

Professional associations:

Approved

Agreed

Scientific Council of the Ministry of Health Russian Federation __ __________201_

Keywords

• Anemia
• Folic acid

Terms and Definitions

1. Brief information

1.1 Definition

Anemia- a state in which the total hemoglobin in the body. The decrease in the concentration of hemoglobin in the blood is a key indicator because it can be measured directly.

1.2 Etiology and pathogenesis

The following factors play a role in the etiology of folate deficiency anemia:

Insufficient intake with nutrition (feeding with goat milk);

Malabsorption in the intestines (enteritis);

Increased need (prematurity; low birth weight; hemolytic anemia, hyperthyroidism, infectious and inflammatory diseases);

The use of medicines - folic acid antagonists (drugs for the treatment of epilepsy, methotrexate);

Increased excretion (hemodialysis).

Isolated deficiency of folic acid is rare, as a rule, it is combined with a deficiency of iron, protein, and other vitamins.

Folic acid is found in green leaves of plants, fruits, liver, kidneys. The stores of folate in the body of an adult are 5-10 mg, the minimum requirement is 50 mcg per day. Megaloblastic anemia can develop after 4 months of complete lack of dietary folate intake.

After ingestion, folic acid is converted into the active metabolite tetrahydrofolic acid, which plays essential role in metabolism nucleic acids and proteins. Folic acid deficiency results in impaired cell division and accumulation of toxic metabolites such as homocysteine.

1.3 Epidemiology

There are no data on the prevalence of folic acid deficiency and folate deficiency anemia in children in Russia.

1.4 ICD-10 coding

folate deficiency anemia(D52):

D52.0 - Dietary folic deficiency anemia

D52.1 Folic deficiency anemia drug-induced

D52.8 - Other folate deficiency anemias

D52.9 - Folic deficiency anemia, unspecified

2. Diagnostics

The clinical picture consists of symptoms characteristic of anemia: weakness, dizziness, shortness of breath, palpitations during exercise, increased fatigue, impaired school performance. Common signs resulting from tissue hypoxia: pallor, tachycardia, shortness of breath, poor appetite, lethargy, or hyperexcitability. In addition, angular stomatitis, glossitis can be observed. Patients may complain of anorexia, nausea, vomiting, abdominal pain, and diarrhea.

Folate deficiency anemia is extremely rare in pure form. As a rule, folic acid deficiency is combined with iron deficiency, since these conditions develop as a result of the action of common etiopathogenetic factors. At the same time and clinical manifestations and laboratory characteristics of anemia depend on the ratio of iron deficiency to folate deficiency. Taking into account that with IDA and with folic deficiency anemia, multidirectional shifts in iron metabolism and erythrocyte indices are observed, laboratory tests with a mixed form of anemia become uninformative. In this situation, the anamnesis and clinic of anemia are crucial.

Differential diagnosis is carried out with vitamin B12 deficiency anemia, other forms of anemia with megaloblastoid type of hematopoiesis: congenital orotataciduria, Lesch-Nyhan syndrome, thiamine-dependent megaloblastic anemia, congenital dyserythropoietic anemia, erythroleukemia. In addition, it is necessary to exclude forms of anemia that occur with macrocytosis, but without signs of megaloblastoidity - aplastic anemia, autoimmune hemolytic anemia, liver disease, hypothyroidism, sideroblastic anemia.

It is necessary to assess the size of the lymph nodes, liver, spleen, exclude the presence of formations in the abdominal cavity, retroperitoneal space, and other signs of malignant diseases.

2.1 Complaints and medical history

It should be noted that with a combined deficiency, the appointment of folic acid without iron preparations will lead to incomplete recovery of hemoglobin and to the manifestation of clinical and laboratory signs iron deficiency. Conversely, if you start treatment with iron supplements, there will be signs of folic acid deficiency.

2.2 Physical examination

General examination involves an assessment of the general physical condition, height and body weight. Pallor is revealed skin, mucous membranes, with severe anemia, there is a rapid heartbeat, shortness of breath.

Because in folic acid deficiency anemia, bone marrow ineffective erythropoiesis occurs and due to this, increased destruction of hemoglobin-containing cells, the level of indirect bilirubin and there is a slight icterus of the sclera and skin. At severe forms there may be a slight enlargement of the spleen (reactive hyperplasia). Thus, there is some similarity between the symptoms of folate deficiency anemia and hemolytic anemia. Laboratory examination allows for a reliable differential diagnosis these forms of anemia.

2.3 Laboratory diagnostics

According to laboratory signs, folate deficiency anemia almost coincides with B12 deficiency anemia. The differences lie in different levels vitamin B12 and folic acid in the blood. In addition, for folic acid deficiency anemia, unlike B12 deficiency anemia, signs of damage are not characteristic. nervous system. It should be remembered that isolated vitamin B12 deficiency in childhood is rare and is usually a complication. helminthic invasion wide tapeworm or hereditary metabolic disorders, as well as the result of exposure to certain medications.

• General clinical analysis blood and biochemical analysis of blood.

Comments:

Folate deficiency anemia is characterized by:

hyperchromia, macrocytosis;

low level of reticulocytes;

high serum iron;

high ferritin levels;

moderate increase in indirect bilirubin;

low levels of folate in the blood serum (the norm is more than 3 ng / ml);

low levels of folate in red blood cells;

normal levels of vitamin B12 in the blood;

picture of megaloblastic hematopoiesis in the bone marrow.

With a combination of iron deficiency and folic acid, combinations of laboratory signs can be observed, which leads to an uncertain picture and difficulty in diagnosis; in this case, it is necessary to focus on clinical symptoms and anamnesis.

High reticulocytosis may be a sign of ongoing bleeding, hemolysis, and is also observed in folic acid deficiency anemia a week after folic acid administration.

Along with anemia, as a rule, there is a moderate decrease in the level of platelets and leukocytes.

Urinalysis is required to rule out proteinuria characteristic of Immerslund-Gressbeck syndrome. To exclude congenital absence internal factor the Schilling test with radioactive labeled vitamin B12 is performed. Given the unavailability of labeled vitamin B12 in general laboratory practice, a modified Schilling test can be used: after ingestion of vitamin B12, the level of vitamin in the blood is determined. In the absence of an increase in the level of vitamin B12, a malabsorption of the vitamin in the intestine is diagnosed.

In the presence of two- or three-linear cytopenia, it is necessary to consider the need for bone marrow examination to exclude leukemia, myelodysplastic syndrome, and aplastic anemia.

The characteristic signs of megaloblastic hematopoiesis in the bone marrow disappear a few hours after taking folic acid.

3. Treatment

• It is recommended that the dosage regimen of folic acid be selected depending on the age of the patient.

Comments: For children of the first year of life, folic acid is prescribed at a dose of 0.25-0.5 mg / kg per day for a month. At an older age, the daily dose is 1 mg / day. oral intake effective even in case of malabsorption, however, in this case, the dose should be increased to 5-15 mg / day.

• It is recommended to monitor blood parameters during treatment:

Complete blood count with counting of reticulocytes, platelets, hematocrit - on the 7th - 10th day from the start of treatment. The presence of a reticulocyte reaction is an important sign of the correctness of treatment.

Control of blood counts once a week. Normalization of the Hb level occurs after 4-6 weeks from the start of treatment and is a decisive confirmation of the correctness of the diagnosis and treatment.

4. Rehabilitation

There are no specific rehabilitation measures for patients with folate deficiency anemia. Dispensary observation carried out taking into account the elimination of the causes of folic acid deficiency (underlying disease, malnutrition).

5. Prevention and follow-up

Proper feeding of infants, the appointment of folic acid to premature babies. Balanced diet older children. Consideration should be given to the possibility of folic acid deficiency in various diseases. Folic acid at a dose of 0.25 - 1 mg / day is prescribed for premature babies, children with low birth weight, children suffering from chronic inflammatory diseases, intestinal diseases with malabsorption syndrome.

Criteria for assessing the quality of medical care

Bibliography

Pediatric hematology / Ed.: A.G. Rumyantseva, A.A. Maschana, E.V. Zhukovskaya. Moscow. Publishing group "GEOTAR Media" 2015 p. 656

whitehead VM. Acquired and inherited disorders of cobalamin and folate in children. Br J Haematol. 2006 Jul. 134(2):125-36.

Duma A, Cartmill C, Blood J, Sharma A, Kharasch ED, Nagele P. The hematological effects of nitrous oxide anesthesia in pediatric patients. Anesth Analg. Jun. 2015 120(6):1325-30.

Dugu? B, Ismail E, Sequeira F, Thakkar J, Gr?sbeck R. Urinary excretion of intrinsic factor and the receptor for its cobalamin complex in Gr?sbeck-Imerslund patients: the disease may have subsets. J Pediatr Gastroenterol Nutr. 1999 Aug. 29(2):227-30

Trakadis YJ, Alfares A, Bodamer OA, et al. Update on transcobalamin deficiency: clinical presentation, treatment and outcome. J Inherit Metab Dis. May 2014 37(3):461-73

Annex A1. Composition of the working group

Rumyantsev A.G. Doctor of Medical Sciences, Professor, Chief Pediatric Hematologist of the Ministry of Health of the Russian Federation Dmitry Rogacheva, Member of the Board of the Union of Pediatricians of Russia, Academician of the Russian Academy of Sciences.

Maschan A.A. MD, Deputy General Director of the Federal State Budgetary Institution FNKTs DGOI them. Dmitry Rogacheva, Professor of the Department of Hematology, Oncology and radiotherapy Faculty of Pediatrics, Russian National Research Medical University named after NI Pirogova, President of the National Society of Pediatric Hematologists and Oncologists, member of the European Society of Hematology.

Demikhov Valery Grigorievich- Doctor of Medical Sciences, Professor, Director of the Scientific and Clinical Center for Hematology, Oncology and Immunology, Ryazan State medical University them. acad. I.P. Pavlov” of the Ministry of Health of Russia, member of the NODGO, member of the European Hematology Association (EHA).

Skobin V.B., Candidate of Medical Sciences, Hematologist, Scientific and Clinical Center for Hematology, Oncology and Immunology, Ryazan State Medical University. acad. I.P. Pavlov" of the Ministry of Health of Russia, member of the NODGO.

Zhurina O.N.., c.m.s., head. laboratory of the Scientific and Clinical Center for Hematology, Oncology and Immunology, Ryazan State Medical University. acad. I.P. Pavlov" of the Ministry of Health of Russia, member of the NODGO.

Conflict of interests missing.

Hematologists

Pediatricians

Doctors general practice

Table P1– Levels of evidence

Table P2– Strength levels of recommendations

Appendix B. Information for Patients

Folic acid deficiency can occur in premature infants, low birth weight infants, and chronic inflammatory diseases, especially malabsorption bowel disease. nutrients. Folic acid deficiency leads to a violation of the formation of red blood cells and a decrease in the level of hemoglobin in the blood. To prevent folic acid deficiency and the development of anemia, it is necessary to provide the child with proper feeding in the first year of life. Breastfeeding is optimal for a child. With absence breast milk should use infant formula that contains all necessary for the child vitamins including folic acid. Feeding goats and cow's milk is one of the causes of anemia. Children at risk (premature, low birth weight, chronic inflammatory disease, intestinal malabsorption syndrome) should be given oral folic acid. Self use drug is unacceptable. Your doctor should prescribe folic acid, taking into account all indications and contraindications.

Paleness has always been synonymous with beauty and aristocracy all over the world. Then no one imagined what iron deficiency anemia was. The Turgenev young ladies did their best to preserve their milky-white skin, and the natural dark-skinned women spent kilograms of white so that no one would guess the natural color of their face. Now times have changed: a healthy, golden face is in fashion.

And fair-skinned women go out of their way to hide their alabaster whiteness by visiting tanning salons, sunbathing on beaches, and so on. However, in order to achieve the desired result, it is first necessary to find out the true cause of this condition. Constant whiteness can indicate problems that have arisen in the body: for example, low blood pressure - and also - serious illness, which will be discussed in detail in this article.

Anemia (anemia) is a condition in which in a unit of blood volume there is a decrease in functionally complete red cells (erythrocytes) and hemoglobin, which leads to oxygen starvation of tissues.

Some of its varieties are hereditary diseases. But more often anemia develops in a person suffering from many other diseases. Quantitatively, it is expressed by the degree of decrease in the concentration of hemoglobin - the iron-containing pigment of erythrocytes, which gives the blood a red color.

The most common types of anemia are: and B ¹² (folic) - deficient. It is on them that questions arise from our readers. These topics are quite extensive, so today we will talk about iron deficiency anemia, but first a few words about what can cause the development of this disease.

1. Diseases of the gastrointestinal tract, manifested by chronic blood loss (or, esophagus, intestines; (inflammation of the esophagus),; and intestinal polyposis; nonspecific;;;.
2. Diseases of the gastrointestinal tract that occur with impaired absorption of iron (resection of the small intestine, enteritis, intestinal amyloid, chronic pancreatitis.
3. Diseases of the liver and its portal tracts with bleeding from dilated veins of the esophagus.

1. Kidney disease with micro- and macrohematuria.
2. Diseases of the cardiovascular system (hypertension with nosebleeds; dissecting aortic aneurysm).
3. Diseases of the lungs and bronchi, occurring with bleeding ( lung cancer tuberculosis, bronchiectasis).
4. Diseases of the blood system (leukemia and hypotactic anemia complicated by bleeding).
5. Hemorrhagic diathesis (thrombocytopenia, hemophilia, hemorrhagic vasculitis).
6. Hypothyroidism (decreased thyroid function).
7. A group of diseases accompanied by intoxication.
8. Menorrhagia ( heavy menstruation) and metrorrhagia (abundant uterine bleeding).
9. Pregnancy and lactation (feeding the baby, nutrition of pregnant and lactating mothers.
10. Insufficient dietary iron intake.
11. Overdonation. As well as acute infections(bacterial, viral, fungal, sepsis, etc.).

Iron deficiency anemia (IDA) is characterized by iron deficiency in the blood serum and bone marrow, which leads to a violation of the formation of hemoglobin and erythrocytes, leading to trophic disorders in the organ and tissues.

Iron deficiency anemia in childhood may be due to prematurity of children, early artificial feeding, frequent infectious inflammatory diseases.

The next form - chlorosis - is early (in young girls) and late (in women 35-45 years old).

Gastroenterogenic chloranemia

For iron deficiency anemia pallor of the skin, drowsiness, taste perversion (tendency to use chalk, clay, egg shells, tooth powder) are characteristic. In the morning increased heart rate, tinnitus, shortness of breath, brittle nails, hair loss.

Patients often complain of stomatitis, cracks in the corners of the mouth, redness and inflammation of the tongue - glossitis, lowering blood pressure.

Iron deficiency anemia can be diagnosed not only in a hospital, but also on an outpatient basis.

When examining a general blood test in patients, the following are revealed: a decrease in the color index, a slight decrease in the number of erythrocytes, an increased content of leukocytes. In a biochemical study of blood, a decrease in iron in the blood is noted.

It consists of several components: medical nutrition, drug therapy and herbal medicine, spa treatment.

Nutrition for IDA

is based on the principles of treatment of the underlying disease - diets No. 1-5, No. 7, No. 10, No. 15.

Iron is best absorbed from animal products (beef meat, veal, beef liver). In addition, I recommend fish, kidneys, lungs, eggs, buckwheat and oatmeal, porcini mushrooms, cocoa, chocolate, greens, vegetables, peas, beans, apples, peaches, kiwi, raisins, prunes, honey, walnuts, dairy products.

Do not forget about the seasonal consumption of vegetables, fruits, berries

Food should be fractional, 5-6 times a day.

Cooking methods: steamed, boiled, baked in the oven, without crust (in the sleeve).

A single serving of the first course should be 250-300 ml + 100-150 g of meat or fish.

A single serving of the second course is 200-250 g of meat, fish + 100-150 g of side dish.

Salads - 100-150 g each, seasoned with 10-15% sour cream (1 tablespoon) or vegetable oil (10-15 ml) + 5-10 ml lemon juice.

One-time reception of wholemeal bread - 100-150 g.

Drinks (tea, compote, fruit drink, chicory) at one time - 200-250 ml.

Freshly squeezed juices should be taken in courses.

Recipe for veal with celery and spices

It will take 4 servings: 750-800 g of veal, 200 g of onion, 350 g of celery, 5 g of salt, 2 pcs. bay leaf, 5-7 peas of allspice, 7 dried fruits of barberry, 7 dried berries juniper, 1/3 teaspoon of anise fruit, 3 clove sticks; a mixture of ground spices (turmeric, cardamom, ginger, nutmeg) - 1/2 teaspoon; 1/2 teaspoon of a mixture of dry herbs (basil, rosemary, oregano, marjoram, coriander); sweet pepper - 100-150 g, fresh parsley - 100-150 g, 200 ml of cream (10%).

Rinse the meat, dry it, chop it, as for goulash (3 cm wide), it is advisable to place it in a cast-iron dish. Sprinkle with chopped onion, chopped celery and sweet pepper. Immediately add all the above seasonings, mix.

Pour 150 ml of cold water, close the lid and put on fire. Let it boil, then reduce the flame as much as possible, simmer over low heat for 45 minutes. Make sure that the liquid does not boil away; constantly pouring water. 10 minutes before full readiness, pour in the cream.

You can choose any garnish.

Conservative therapy

Drug therapy with iron-containing preparations for each patient is selected by the doctor, based on the results of various studies. I will just list some of these drugs taken by mouth: ferronat, heferol, ferlatum, ferrograd, ferroplex, irradian, tardiferon, maltofer, ferrum-lek and etc.

There are also drugs that are administered intramuscularly and intravenously - they are also individually prescribed by a specialist.

Phytotherapy - folk recipes

Reception herbal preparations it would also be good to discuss with a phytotherapist.

Gathering #1

We will need 3 parts, 5 parts, 2 parts of leaves. Mix the ingredients, grind, preferably in a coffee grinder. Place in a glass dish. Store in a dry, dark place.

1 dec. place a spoonful of the mixture without top into glass jar, pour 500 ml of boiling water, leave for 7 hours, strain, store in the refrigerator. Take 150 ml warm 1.5 hours after meals 3 times a day. You can add honey to taste.

The course of admission is a week. Then increase the dose of the herbal mixture to 1 tbsp. spoons, preparation and reception left unchanged. Drink for another 5 days, take a break for 2-3 weeks and the treatment can be repeated.

Gathering #2

Take the leaf, flowers and crushed root equally. Mix the components, store in the same way as the previous collection.

Place 1 tablespoon of the collection in an enameled saucepan, pour 500 ml of boiling water, put on a slow fire, boil for 5 minutes, leave for 3 hours, strain, store in the refrigerator.

Take warm 30 minutes before meals, 150 ml 3 times a day, adding honey to taste. The course is 6-8 weeks.

The reception of these fees can be alternated, conducting 2-3 courses per year.

After receiving a positive effect in the treatment, it is desirable to conduct a sanatorium treatment in Kislovodsk, Essentuki, Zheleznovodsk, etc.

E.S.Sakharova, E.S.Keshishyan, CONSILIUM Medicum 2002, Appendix: Pediatrics

Anemia is one of the most common pathologies in children. early age. About 20% of full-term children suffer from this disease, and among premature babies in the first year of life, almost everyone develops anemia. At the same time, the severity of anemia is the higher, the lower the gestational age of the child. In the first months of life in premature babies with very low birth weight (less than 1500 g) and a gestational age of less than 30 weeks. severe anemia requiring red blood cell transfusion is up to 90%.
In the pathogenesis of early anemia of prematurity, not only the formation of iron deficiency, which is characteristic of all young children, but also factors of incomplete ontogenesis play a role.
Hematopoiesis in the prenatal period begins very early. Already in the first 2 weeks. development of the embryo, islets of hematopoiesis are determined - erythrocytes are produced yolk sac. Starting from 12-16 weeks, the main place of hematopoiesis becomes the liver and, to a lesser extent, the spleen. Approximately at 20 weeks. prenatal development the fetus begins erythropoiesis in the bone marrow, and gradually fades in the liver and spleen. Thus, by the time of birth in full-term children, hematopoiesis in the liver almost completely stops, while in very preterm infants, hematopoietic foci remain almost until the 40th week of gestation (i.e., from 3 weeks to 3 months of their actual age). In the early stages of intrauterine development, a small amount of erythrocytes. Before the onset of bone marrow hematopoiesis, the concentration of erythrocytes in the blood of the fetus grows slowly, and by the time of birth it increases sharply and is already 5-6 million per 1 mm 3.
Premature babies are characterized by morphological changes in erythrocytes. So, erythrocytes of an abnormal form make up 27%, while in full-term newborns it is only 14%. This contributes to the fact that the period of life of an erythrocyte in full-term infants is almost 2 times longer than in premature infants, and is 60-70 and 35-50 days, respectively.
Shortening the life of erythrocytes can contribute to the structural features of their membranes. When studying the composition of total lipids of erythrocyte membranes in children with early anemia of prematurity, it was found that from the 2nd week they have a decrease in the content of phospholipids and an increase in cholesterol. These changes progress to the 6th week of life and reach a maximum at the height of anemia, which correlates with clinical and laboratory symptoms.
In violation of the permeability of erythrocyte membranes in premature infants, a low level of vitamin E also plays a role, which is localized in the membranes and is actively involved in peroxide phosphorylation. Vitamin E deficiency is observed in 86% of premature babies.
The fetal erythrocytes early stages ontogeny produce the germinal (embryonic) form of hemoglobin.
Between 7-12 weeks of intrauterine life, fetal hemoglobin is replaced by fetal hemoglobin. The hemoglobin level also depends on the gestational age, averaging 90 g/l at the 10th week, and 170±20 g/l by the 38th week.
Fetal hemoglobin has a higher affinity for oxygen and a slower release of oxygen to tissues compared to adult hemoglobin. Switching the synthesis of fetal hemoglobin to adult hemoglobin is under the control of genes located on the 11th and 16th chromosomes and begins at the 30th-32nd week of intrauterine development. The content of fetal hemoglobin in premature babies at birth averages 70-80%, in full-term newborns - 60-70%. More than half of the volume of fetal hemoglobin is replaced by adult hemoglobin in the first days of a child's life, then this process slows down somewhat, but by the 4-5th month of postnatal life, most children have about 1% of fetal hemoglobin. In premature babies, this process is slowed down, the main volume of hemoglobin change falls on the 40th week of gestation, and a complete change stretches for almost the entire first year of life. In addition, the delay in switching synthesis from fetal hemoglobin to adult hemoglobin is enhanced by severe hypoxia and fetal stress.
The hematocrit level is determined by the concentration of hemoglobin and red blood cells in the blood. Normally, the hematocrit in newborns is higher than in adults, and is 50-55%.
A reflection of the state of erythropoiesis is the level of reticulocytes. The average number of reticulocytes in a newborn is 4.2-7.2%. At the end of the 1st week of postnatal age, this figure decreases to the level of adults and is 1%.
At the birth of a full-term baby, a high hemoglobin content is determined, which, under conditions of increased oxygen consumption compared to intrauterine oxygen consumption, is excessive. This, in turn, leads to an increase in the production of erythropoietin and a decrease in erythropoiesis. With suppression of bone marrow function and increased destruction of erythrocytes, there is a gradual decrease and change in hemoglobin, which reaches 110-120 g / l in full-term children by the 8-12th week. If hemoglobin decreases to this threshold - for full-term 100-110 g / l, oxygen delivery to tissues is disturbed, which stimulates the production of erythropoietin. As a result, the process of increasing the production of erythrocytes begins.
In premature babies, the process of destruction of erythrocytes is faster due to more short period the life of these cells. The level of hemoglobin, at which the production of erythropoietin begins to increase in premature babies, is significantly lower than in full-term babies, and is 90-70 g / l (thus, such a hemoglobin level - critical for full-term babies, is acceptable for premature babies!).
In adults and older children, in response to even mild hypoxia, a rapid increase in erythropoietin production is observed, while preterm infants are not able to produce adequate amounts of erythropoietin even at critical values ​​​​of circulating erythrocytes, which is apparently due to a lower oxygen demand.
Thus, anemia of prematurity is characterized by a progressive decrease in hemoglobin levels (up to 90–70 g/l and below), a relatively low level of reticulocytes, and inhibition of bone marrow hematopoiesis.
Allocate early and late anemia of prematurity.
Early anemia develops on the 4th-10th week of postnatal life and is characterized by a decrease in the level of reticulocytes of less than 1%, the level of hemoglobin to 80-70 g/l and below, and the hematocrit to 20-30%.
The clinical picture of early anemia of prematurity is manifested by symptoms characteristic of true anemia, such as pallor of the skin, tachycardia or bradycardia, tachypnea, and apnea.
Among the causes of early anemia of prematurity, in addition to those indicated, a certain importance is attached to the high rate of increase in body weight and volume of circulating blood, incommensurable with the level of erythropoiesis.
In addition, the deficiency of folic acid, vitamin B6, microelements: zinc, copper, selenium, molybdenum plays a role in the genesis of early anemia of prematurity. Stocks of folic acid are depleted during the first weeks of life, which leads to a violation of the synthesis of folate by the intestinal microflora.
It is known that early anemia of prematurity can be one of the manifestations of infection and be potentiated by its postnatal development.
There are studies proving the relationship between the concentration of hemoglobin and the level of thyroid hormones (T3 and T4). Under conditions of a relative deficiency of T3 and T4, characteristic of premature babies, there is a violation of those stages of erythropoiesis that require intensive synthesis of specific proteins - enzymes involved in the formation of hemoglobin.
In addition to the "conditionally physiological" causes of anemia associated with incomplete ontogenesis, unfortunately, so-called iatrogenic causes play a certain role in potentiating the severity of anemia, such as frequent, albeit small in volume, blood loss as a result of blood sampling for laboratory research without replenishment of the BCC. According to the literature, during the first week of life, about 38.9 ml of blood is taken from a newborn premature baby for research. Relative to the total blood volume (80 ml/kg of weight), this is a very large figure.
Summarizing all that has been said, a combination of several factors play a role in the pathogenesis of anemia of prematurity:
a) shortened life span of erythrocytes;
b) prolonged circulation and late change of fetal hemoglobin;
c) the peculiarity of the metabolism of proteins, vitamins, microelements;
d) infectious agents, in particular gram-negative flora, for the vital activity of which an active consumption of iron is necessary;
e) iatrogenic causes.
One of the main methods of treatment of early anemia of prematurity is still blood transfusions. The most commonly used blood transfusions are donated red blood cells. Indications for red blood cell transfusions in anemia of prematurity are: decrease in hemoglobin below 130 g/l and hemotocrit below 0.4 during early adaptation (the first 7 days of life) in combination with severe respiratory and cardiac disorders. The widespread use of blood transfusions in premature infants is associated with a low but significant risk. First of all, this is the possibility of transmission of viral infections (HIV, CMV) with transfusions, it is also possible to overload the vascular bed with fluid, the development of the "graft-versus-host" state, and electrolyte imbalance. Currently, alternative ways of solving this problem are being searched. One of them is the use of recombinant human erythropoietin, the effectiveness of which is now being intensively studied.
Late anemia of prematurity develops at the 3-4th month of life. It is more similar to iron deficiency anemia in young children. The clinical picture of late anemia of prematurity is characterized by decreased appetite, flattening of the weight curve, pale skin and mucous membranes, dry skin, enlarged liver and spleen. There is a decrease in serum iron - hypochromia, with a tendency to microcytosis and a hyperregenerative reaction of the bone marrow.
In addition to all the features inherent in early anemia of prematurity, during the development of late anemia, symptoms of iron deficiency begin to appear. The most active intake of iron from mother to fetus is carried out in the last 2 months. pregnancy, so prematurity at 4-8 weeks. can lead to a reduction in iron stores by 1.5-3 times compared with full-term.
In full-term babies, the reticuloendothelial system has a 15-20 day supply of iron. As soon as the lower level of hemoglobin is reached - 100-110 g / l in full-term and 70-90 g / l in premature, stimulation of erythropoiesis begins. If iron stores are insufficient, there is a further decrease in hemoglobin and anemia becomes iron-deficient. In a premature baby, the need for iron is higher than in a full-term baby, and there are strikingly fewer reserves. Given that iron is found in the body not only in the form of heme, but also goes to the construction of myoglobin and enzymes - catalase, peroxidase, cytochromes and cytochrome oxidase, its postnatal consumption is extremely high.
After birth, sources of iron for developing organism are the intake of exogenous iron in the composition food products and its utilization from endogenous reserves.
Attempts to enrich the diet with the introduction of adapted mixtures, including those enriched with iron, do not lead to the desired result, since the latter is poorly absorbed. For premature babies, especially in the first months of life, the only physiological food that ensures the balance of iron metabolism in the body is mother's milk, balanced for all ingredients in accordance with physiological needs growing organism. Although the content of iron in women's milk is low (0.2-1.5 mg / l), there are special mechanisms for its more efficient absorption (up to 50%). At the same time, a big problem is the maintenance of lactation in women who are under stress as a result of prematurely terminated pregnancy and a sick child. Educational work, psychological support for the mother are the only way to provide breastfeeding for a premature baby.
For dietary correction iron deficiency requires timely (but not earlier than the 4-5th month of life) the introduction of complementary foods (fruits, vegetables, later, after 8 months - meat). At the same time, studies have shown that for the treatment of anemia (but not for its prevention), it is not enough just to increase the level of dietary iron, but a drug subsidy is required.
Why is iron deficiency anemia so dangerous?
Iron deficiency anemia contributes to the development of chronic hypoxia, which in turn can lead to a slowdown in the mental and psychomotor development of the child.
In this regard, the treatment of anemia in preterm infants and the prevention of iron deficiency in all children is important and mandatory. integral part in general scheme observation of children in the 1st year of life. In addition to important dietary approaches, the early administration of prophylactic doses of iron preparations to all premature babies is relevant. The drugs of choice in this case are modern representatives of the hydroxide polymaltose complex of ferric iron: Maltofer and Ferrum Lek. Hydroxide polymaltose complex is stable under physiological conditions, which excludes the formation of free iron ions. Unlike the previously common salt (ionic) iron preparations - divalent compounds of iron salts (for example, ferrous sulfate), polymaltose complexes (Maltofer and Ferrum Lek) do not irritant on the intestinal mucosa, which often manifests itself in the form of constipation, diarrhea, nausea, regurgitation. The absorption of iron from polymaltose complexes is close to the absorption of heme iron and is provided by an active transport mechanism, the most physiological for the body. AT this case iron is directly transported through transferrin receptors to hematopoietic sites or delivered to iron storage sites, where it is deposited in the reticuloendothelial system (liver and spleen) in the form of ferritin.
Clinical researches of the drug "Maltofer" showed its equal effectiveness in comparison with salt preparations. At the same time, the number of side effects from the gastrointestinal tract is 3 times less with the use of the iron polymaltose complex, and the number of patients who refused to continue the course of treatment is more than 2 times more in the group of salt preparations.
Chemical structure The complex does not release free iron. Together with the active transport mechanism of iron absorption, this protects the body from intoxication with free iron ions, as well as their oxidative effects, inherent in iron salt preparations.
The same mechanisms support the system of self-regulation according to the principle " feedback": the absorption of iron from the complex stops as soon as its required level in the body is restored, which eliminates the possibility of poisoning with these drugs in case of their overdose.
Premature infants from the first weeks of life up to the 1st year are recommended to take these iron preparations prophylactically at the rate of 2 mg/kg/day of elemental iron. The therapeutic dose is 5 mg / kg / day of elemental iron and does not change until the hemoglobin level normalizes. Monitoring of red blood parameters (hemoglobin level, CP, erythrocytes) in premature babies after discharge from the nursing departments should be carried out in without fail at 3, 6 and 12 months, then 2 times a year, and if anemia is detected, every 14 days until the hemogram parameters stabilize.
Taking into account the peculiarities of the pathogenesis of anemia in premature infants, the tendency to develop a hyporegenerative reaction of the bone marrow, megaloblastosis, macrocytosis, increased hemolysis of erythrocytes, children with low birth weight at birth need early, from 7 days of life, the introduction of folic acid 1 mg per day, vitamin E 20 mg/kg per day, B vitamins.
According to the Order of the Ministry of Health of the Russian Federation No. 375 dated 12/18/97 on conducting preventive vaccinations iron deficiency anemia is not a contraindication to vaccination. On the other hand, premature babies are special group risk for the development of a complicated infectious process. Therefore, even in the case of severe manifestations of anemia, preventive vaccinations can be carried out immediately after stopping. acute manifestations. A moderate decrease in hemoglobin, antianemic treatment is not a reason to postpone vaccination.

Literature

1. Bisyarina V.P., Kazakova L.M. Iron deficiency anemia in young children. M., 1979; 176.
2. Nex E., Cristensen N.S., Olesen S. Volume of blood removed for analytical purposes during hospitalization of low birth weight infants. Clinical chemistry, 1981; 27:759-61.
3. Aldysheva T.V. The combination of substances in blood plasma and the activity of antioxidant enzymes in erythrocytes in the presence of anemia in premature babies. Issues of adaptation of premature babies and children infancy. M., 1985; 127-30
4. Degtyarev D.N., Kurmasheva N.A., Volodin N.N. Modern ideas about the pathogenesis and treatment of anemia in premature babies. Lectures of the department of neonatology of the Russian State Medical University, 1994.
5. Dallmann P.R. Nutritional anemia in infancy in Tsang R.C., Nicols B.L. Nutrition during infancy, Philadelphia, 1988.
6. Krasnitskaya L.N. The content of thyroid hormones, testosterone and cortisol in the blood serum of premature infants with early anemia. Abstract diss. Candidate of Medical Sciences, L., 1988; 22.
7. Prigogina T.A. The efficacy of recombinant erythropoietin in comprehensive prevention and treatment of early anemia of prematurity. Diss. Candidate of Medical Sciences, M., 1988.
8. Akre D. Feeding children of the first year of life: functional bases. WHO Bulletin, 1989; appendix to volume 67: 30-35.
9. Walter T. Infancy: mental and motor development. American Journal of Clinical Nutrition, 1989; 50:655-66
10. Jacobs P. et. al. Better tolerance of iron polymaltose complex compared with ferrous sulfate in the treatment of anemia. Hematology, 2000; 5:77-83
11. Geisser P. et. al. Structure / histotoxicity relationship of oral iron preparations. Drug Research, 1992; 42:1439-52.
12. Tuomainen, T-P, et al. Oral supplementation with ferrous sulfate but not with non-ionic iron polymaltose complex increases the susceptibility of plasma lipoproteins to oxidation, Nutrition Research, 1999; 19:1121-32
13. Geisser P., Hohl H. and Mueller A. Klinische Wirksamkeit dreier verschiedener Eisenpraeparate an Schwangeren. Switzerland. Apotheker-Zeitung, 1987; 14:393-8
14. Fedorov A.M. About the new calendar of preventive vaccinations. children's doctor, 1999; 1: 27-9.

FOR GENERAL PRACTITIONERS
IRON-DEFICIENCY ANEMIA

2. Codes according to ICD-10

3. Epidemiology

4. Factors and risk groups

5. Screening

6. Classification

7.Principles of diagnosing the disease in outpatient settings

8. Criteria for early diagnosis

9. General principles outpatient therapy

10. Indications for blood transfusion

11. Indications for a consultation with a hematologist

12. Indications for hospitalization of the patient

13. Prevention

14. Forecast
Bibliography
tables

List of abbreviations
ACHD - Anemia of chronic diseases

IDA - iron deficiency anemia

GIT - gastrointestinal tract

CBC - complete blood count

TIBC - total iron-binding capacity of blood serum

Fl - flavone (cubic micrometer)

CPU - color index
HB - hemoglobin

MCV - mean corpuscular volume - the average corpuscular volume (size) of an erythrocyte
1. Definition.

Iron deficiency anemia (IDA)- anemia associated with impaired hemoglobin synthesis as a result of a decrease in iron stores in the body.
2. Codes according to ICD-10

D50 Iron deficiency anemia

D 50.0 Iron deficiency anemia secondary to blood loss (chronic)
3. Epidemiology.

Iron deficiency anemia is the most common form of anemia, accounting for more than 80% in all regions. IDA is most common in young children and women childbearing age. In Europe and North America, iron deficiency anemia affects 10-20% of women of childbearing age; in Africa, Latin America and Asia - 50-60%. The probability of developing iron deficiency anemia in women with heavy menstruation reaches 80%.

The total loss of iron in a woman at the birth of one child is 1200-1400 mg (fetal formation, transport to the placenta, blood loss during childbirth, lactation). It takes at least 1.5 years to replenish iron reserves. It is this period of time after the end of lactation that is most appropriate for planning the next pregnancy.

IDA is very common in infants. This is due to the fact that with improper feeding (nutrition with low content iron) after 5-6 months, the child depletes the supply of iron received from the mother in the prenatal period.

In menopausal women, the frequency of IDA is the same as in men (3-4%).
4. Factors and risk groups.

Table 1

Risk factors for developing IDA

5. Screening.

For IDA screening, clinical data can be used: the presence of sideropenic syndrome (taste perversion, changes in skin appendages, etc.) in combination with risk factor data (see above) and complete blood count (CBC) data. KLA data indicating the possible presence of iron deficiency anemia include a low color index (cp less than 0.86) and a low mean corpuscular volume of an erythrocyte (MCV less than 80 fl). If IDA is suspected, a study of iron metabolism parameters should be carried out.
6. Classification.

Iron deficiency anemia is not an independent nosological form, but a syndrome that can develop in many diseases accompanied by chronic blood loss or malabsorption of iron; and with vegetarianism.

IDA is the result of a long-term negative iron balance. There are three stages in the development of iron deficiency anemia:

1. 
   Prelatent iron deficiency;
2. 
   Latent iron deficiency;
3. 
   Actually iron deficiency anemia, i.e. decrease in the level of HB less than 120 g / l.

chronic iron deficiency anemia allows its timely diagnosis.

table 2

Stages of development of iron deficiency

Depending on laboratory parameters, three degrees of severity of iron deficiency anemia are distinguished:

mild - hemoglobin level (HB) more than 90 g / l,

medium - hemoglobin from 70 to 90 g / l

severe - the level of HB is less than 70 g / l.
Iron deficiency anemia is chronic. Due to the slow rate of decrease in hemoglobin, the condition of patients usually remains satisfactory even with a decrease in the level of HB less than 70 g / l, especially at a young age.
Diagnosis example

Example: Iron deficiency anemia of severe severity.
7. Principles of diagnosis of the disease in adults on an outpatient basis.
In the presence of anemia, it is necessary to perform an expanded CBC with platelets, reticulocytes and leukocyte formula.

In most cases, the diagnosis of iron deficiency anemia is not difficult. For this, clinical data are sufficient (the presence of a probable source of blood loss and sideropenic syndrome), a study of peripheral blood with the determination of a color index (its decrease is typical) and / or erythrocyte indices (MCV, MCH, MCHC - their decrease is characteristic), a decrease in the level of serum iron, and also increase the total iron-binding capacity of blood serum (OZHSS) and reduce the level of serum ferritin.

In women of childbearing age, the most likely source of blood loss is menstrual blood loss. Blood loss exceeds physiological (300 ml) if at least one of the following signs occurs: the duration of menstruation exceeds five days; in the secretions, the presence of clots is noted; More than 10 pads/tampons are used per period.

In men, the most likely is the presence of latent blood loss from the gastrointestinal tract (GIT). The sources of this can be attributed, first of all, chronic hemorrhoids. In this case, blood loss can be minimal, not attracting the attention of the patient, but its duration of many months leads to the gradual formation of a negative iron balance and the development of iron deficiency anemia. Other sources of blood loss from the gastrointestinal tract include diverticula, polyps, hernia esophageal opening diaphragm, gastric and duodenal ulcers, ulcerative colitis, Crohn's disease, etc.

Sideropenic syndrome develops with iron deficiency in tissues. Its main clinical signs are taste perversion (addiction to calcium gluconate, etc.), addiction to strong odors, deformation, thinning and delamination of nails, hair loss, dysphagia, urinary incontinence in women.

The most important for the differential diagnosis of anemia and determining the plan for further examination is the determination of the color index and erythrocyte indices.

The color indicator reflects the relative content of hemoglobin in one erythrocyte in conventional units. It is calculated by dividing the hemoglobin concentration by the number of red blood cells in the blood according to the formula:

Cp \u003d 3 * HB (g / l) / the first three digits of the number of erythrocytes

For example, hemoglobin is 140g/l, erythrocytes are 4.2*10/12/l. CPU \u003d (3 * 140) / 420 \u003d 1.0.

Normally, the color index is in the range of 0.86-1.05. Depending on the size of the cp, hypochromic (cp less than 0.85), normochromic (cp 0.86-1.05) and hyperchromic (cp more than 1.05) anemia are distinguished. Iron deficiency anemia refers to hypochromic anemia.

The mean corpuscular volume of erythrocytes (erythrocyte size) (MCV-mean ctll volume) is the most valuable indicator for the differential diagnosis of anemia. Calculate MCV using the following formula:

MCV = hematocrit (%) * 10 / number of red blood cells in millions per 1 mm3

For example, hematocrit 40%, red blood cells 4.7 * 10/9. Therefore, MCV will be (40*10):4.7=85 µm3. The normal MCV is 80-95 fl.

Based on MCV, anemias are divided into normocytic (MCV within 80-95 fl), microcytic (MCV less than 75 fl) and macrocytic (MCV more than 95 fl). Iron deficiency anemia is a microcytic anemia.

differential diagnosis.

AT practical work it is necessary to differentiate iron deficiency anemia from other microcytic hypochromic anemias, which include anemia of chronic diseases, sideroblastic anemias, and heterozygous thalassemias. This must be remembered, since iron preparations have a positive effect only with iron deficiency anemia. In other microcytic hypochromic anemias, the use of iron preparations is useless, and with long-term use in high doses (especially parenteral administration) is even harmful, as it can lead to the development of secondary hemosiderosis.

Anemia of chronic diseases (ACD) often develops in chronic inflammatory, autoimmune, infectious diseases, malignant neoplasms. Most patients have normochromic normocytic anemia, but in some cases moderate microcytosis and hypochromia are possible. In anemia of chronic diseases leading to clinical picture are manifestations of the underlying pathology ( infective endocarditis, rheumatoid arthritis, etc.), there is no sideropenic syndrome, anemia is moderately expressed (hemoglobin is usually in the range of 90-100 g / l). The content of serum iron in ACD can be slightly reduced, however, in contrast to iron deficiency anemia, there is also a decrease in the level of total and unsaturated transferrins with a normal ferritin content.

Sideroblastic anemia is characterized by the absence of sideropenic syndrome, qualitative disorders of erythropoiesis, leukopoiesis and megakaryocytopoiesis, an increase in the number of sideroblasts in the bone marrow and the appearance of their ring-shaped forms, an increase in the content of iron and ferritin in the blood serum. Allocate congenital and acquired forms of sideroblastic anemia. In the latter case, it can be an independent nosological form (a variant of myelodysplastic syndrome), or be associated with other diseases (solid tumors, leukemia), alcoholism, copper deficiency, treatment with certain medications (levomycetin, isoniazid).

Heterozygous beta thalassemia is an inherited hemolytic anemia. In Russia, this disease occurs more often among the indigenous people of the North Caucasus, but it also occurs in people of other nationalities. The main criteria for diagnosis is an increase in the level of hemoglobin A2 and F during hemoglobin electrophoresis. In the peripheral blood, pronounced microcytosis, an increase in the number of target erythrocytes, serum iron, total and unsaturated transferrins and ferritin are noted.
8. Criteria for early diagnosis.

Identification of patients with iron deficiency at an early stage, that is, at the stage of latent iron deficiency, is associated with a number of difficulties. At this stage, patients often do not seek medical help due to the lack of limitation of exercise tolerance. In this case, patients do not have anemia, but only sideropenic complaints (taste perversion, changes in skin appendages, etc.), which must be actively identified if risk factors are present.

If a latent iron deficiency is detected, it must be treated, otherwise it will transform into iron deficiency anemia. For therapy, a diet rich in red meat and the same drugs are used as for the treatment of IDA, but their dose is halved (up to 1 tablet per day).
9. General principles of outpatient therapy

For successful treatment iron deficiency anemia, it is necessary to establish and, if possible, eliminate its cause (reduce the volume of menstrual blood loss, remove hemorrhoids, etc.). The diet should contain a sufficient amount of iron, that is, 100-200 mg of red meat per day. It is necessary to explain to the patient that sausages, chicken, broths, etc. do not belong to red meat. a complete diet prevents the progression of iron deficiency, but cannot eliminate anemia that already exists.

For the treatment of IDA, a prescription is required medications. Oral iron preparations are an effective and well-tolerated treatment for patients with iron deficiency anemia. Iron preparations are usually prescribed in the form of sulfate or fumarate. The most well-known drugs are sorbifer (iron sulfate containing 100 mg of iron and ascorbic acid), fenyuls (iron sulfate (45 mg) with ascorbic acid and riboflavin), maltofer (iron-polymaltose complex) and ferrum-lek (iron-polymaltose complex). Ferroplex deserves attention, since it contains only 10 mg of iron and to achieve therapeutic effect it is necessary to take 8-10 tablets per day.

Adults should be given 200 mg of iron per day. Taking a single dose of more than 150 mg and daily dose more than 450 mg does not lead to an increase in its intake into the body. Ferrous sulfate (sorbifer, fenules) should be taken on an empty stomach, half an hour before meals, as food reduces iron absorption by 40-50%. Preparations of the iron-polymaltose complex can be taken regardless of food intake. When taking these drugs, dyspeptic syndrome as a side effect practically does not occur.

Starting dose 1 tablet 2 times a day for a month.

The condition of patients on the background of treatment with iron preparations often improves by the end of the first week, however, a clear increase in the levels of HB and erythrocytes usually begins after 2.5-3 weeks, so the control of the KLA earlier than 4 weeks from the start of treatment does not make sense. Normalization of hematological parameters occurs after 4-6, and in severe anemia and after 8 weeks.

A month after the start of taking iron supplements, the patient comes to the control visit with a general blood test. Therapy is considered adequate if, by the end of the third week of treatment, the level of HB rises to a mark that is the middle between the initial and normal levels.

In the presence of positive dynamics in the KLA after 1 month, it is necessary to continue taking iron supplements at a therapeutic dose (1 t * 2 times a day) with the control of the KLA every month until the level of HB rises more than 120 g / l. This usually takes 2 to 4 months. A typical mistake is to stop taking iron supplements until the level of HB normalizes, since the patient's well-being normalizes very quickly. However, this leads to a recurrence of anemia. After the level of HB is normalized, iron preparations are not canceled, but their dose is only reduced to 1 tablet per day. At this dose, the patient takes iron supplements for another 2-4 months, depending on the initial depth of anemia, in order to replenish the depot. If the source of blood loss cannot be eliminated at the same time (for example, polymenorrhea), then a constant monthly intake of iron preparations is recommended on the days of the menstrual cycle.

In some cases, treatment with oral iron preparations is ineffective, which may be due to:

ongoing blood loss

Incorrect intake or inadequate dose of the drug

Misdiagnosis (anemia of chronic disease, thalassemia, sideroblastic anemia).

Combined deficiency (most often iron and vitamin B12)

Iron malabsorption.

Parenteral iron preparations are more effective than oral iron preparations, however, they are more often accompanied by the development adverse reactions sometimes life threatening. Indications for the appointment of parenteral iron preparations:

Intolerance oral medications gland

The need for rapid replenishment of iron stores (severe IDA, postoperative period, last weeks of pregnancy, rebleeding in hemorrhagic diseases)

Gastrointestinal diseases (UC, Crohn's disease)

Iron malabsorption

Chronic hemodialysis.

Parenteral iron preparations are preferable to be administered intravenously, since intramuscular injection less effective (part of the iron is deposited in the muscles in the form of hemosiderin) and may be complicated by the development of post-injection infiltrates. Begin treatment with a trial dose of drugs (1/2 ampoules), which is administered very slowly. The most common parenteral iron preparations are ferrum-lek and venofer. The intravenous form of the preparations contains 5.0 ml of the medicinal substance, the intramuscular form of ferrum-lek - 2.0 ml. Parenteral iron preparations are prescribed 1 injection every other day (on an outpatient basis - Monday, Wednesday, Friday). Side effects when treated with iron preparations, they develop in 10-20% of patients (when treated with venofer less often than when treated with ferrum-lek). The most common are:

Nausea

Increase in body temperature

Arthralgia

Pain and infiltrates at injection sites (with intramuscular injection)

Allergic reactions (up to anaphylactic shock).
Criteria for the effectiveness of treatment with oral or parenteral preparations gland:

Improvement of the general condition of the patient by the end of the first week of treatment

Increase in the number of reticulocytes up to 30-50%% in 5-10 days

An increase in hemoglobin (usually begins after 2-3 weeks), the hemoglobin level returns to normal after 4-5 weeks.

Improvement of the qualitative composition of erythrocytes (microcytosis and hypochromia disappear)

Gradual regression of epithelial changes.
10. Indications for blood transfusion.

RBC transfusions are carried out only according to vital indications. If the HB level is less than 70 g/l, blood transfusion is carried out ONLY if anemia is accompanied by clinical signs of tissue hypoxia (severe tachycardia, tachypnea) or before surgery. In older patients, indications for packed red cell transfusions (i.e. signs of hypoxia) may also occur at higher hemoglobin levels. With satisfactory health, no signs of hypoxia, disorders of the cardiorespiratory system and a favorable prognosis (chronic iron deficiency anemia in the absence of signs of ongoing blood loss), pathogenetic and symptomatic treatment without transfusions of the er.mass, it can also be carried out with severe anemia. The frequency of blood transfusions is determined depending on clinical and laboratory parameters.
11. Indications for a consultation with a hematologist.

Indications for consulting a hematologist are difficult cases when it is difficult to conduct differential diagnosis on an outpatient basis with such diseases as thalassemia, sideroblastic anemia. Indications for referral to a consultation with a hematologist may also be the absence of positive dynamics after a month of ferrotherapy, provided that the patient has undergone a study of iron metabolism indicators before starting treatment. “Blind” treatment tactics can be considered unsatisfactory, when a patient without additional examination, on the basis of a general blood test alone, is “automatically” prescribed iron supplements, which after a month of admission are ineffective. In this case, their further intake is meaningless, it is also meaningless to prescribe additional vitamin B12 or folic acid without a confirmed diagnosis. This tactic complicates the diagnostic search, lengthens the diagnostic period, and leads to loss of time and money. If the patient takes several drugs without effect, it is necessary to stop treatment and repeat the examination of the patient no earlier than after 7 days.
12. Indications for hospitalization of the patient.

Severe signs of tissue hypoxia (need for blood transfusion)
13. Prevention.

For patients at risk, as well as patients who have recovered from IDA, a diet rich in red meat is recommended: 100-200 mg of red meat at least 5 times a week. With a continuing source of blood loss (polymenorrhea), iron preparations are justified monthly for 5-7 days.

14. Forecast.

With proper treatment, elimination of the source of blood loss, the prognosis is favorable.
Bibliography.

1. 
   Novik A.A., Bogdanov A.N. Anemia (from A to Z). A guide for doctors / edited by acad. Yu.L. Shevchenko. - St. Petersburg: Publishing House "Neva", 2004. - 320 p.
2. 
   Hematology / edited by Prof. Rukavitsyn O.A. - St. Petersburg: LLC "D.P.", 2007. - 912 p.
3. 
   Rational pharmacotherapy of diseases of the blood system: A guide for practicing physicians. – M.: Littera, 2009. – 688 p.

tables

Table 1. Risk factors for iron deficiency anemia.

Table 2. Stages of development of iron deficiency.

ANEMIA - literal translation from Greek - bloodlessness, anemia (anaemia; "an" - without, "haima" - blood), in the clinical sense: Anemia - pathological condition, characterized by a decrease in hemoglobin content, often in combination with a decrease in the number of red blood cells per unit volume of blood.

Iron deficiency anemia, unlike most other anemias, is often not accompanied by a decrease in the content of erythrocytes per unit volume of blood.

According to WHO recommendations (1973), the lower limit of Hb should be considered 110 g/l in children under the age of 6 years and 120 g/l in children over 6 years of age. At the same time, GF Sultanova (1992) draws attention to the fact that WHO experts determined the normative parameters of hemoglobin by analyzing venous blood samples. In everyday practice, basically, the level of hemoglobin is determined by examining capillary blood. The content of Hb in capillary blood is 10-20% higher than in venous blood (Todorov I., 1966). Considering this, normally the values ​​of hemoglobin in capillary blood should not be lower than 121-132 g/l (Sultanova G.F., 1992). Yu.E. Malakhovskiy (1981) also believes that the optimal level of hemoglobin for children under 6 years of age is above 120 g/l, and for children over 6 years of age - above 130 g/l. The lack of uniform criteria in assessing the lower level of normal hemoglobin values ​​often leads to erroneous conclusions in the Diagnosis of anemia (Basova L.V., 1975; Volosyanko R.P., 1972; Kyshtobaeva S., 1974; Myakisheva L.S., 1971; Sultanova G.F., 1992).

2.2. The frequency of iron deficiency anemia in children.

Iron deficiency anemia is widespread in the pediatric population and is the most common form among all childhood anemias. According to WHO (1985), almost 30% of the world's population has iron deficiency, in varying degrees of severity. The greatest risk of developing iron deficiency anemia, especially in developing countries, and this is emphasized by most researchers, have children of early and pubertal age, as well as women of the childbearing period (Table 4)

Table 4

Prevalence of iron deficiency anemia by age, sex and region (%)*

In the children's population of the former USSR, the prevalence of iron deficiency (latent and manifest clinical forms) ranged from 17.5% in schoolchildren to 76% in young children (Babash G.V. et al., 1980; Kazakova L. M. et al. ., 1984; Malakhovskiy Yu. E. et al., 1981; Yudina T. N., 1989). However, the true frequency of iron deficiency anemia in the pediatric population is unknown, because given by different authors, its prevalence ranges from 5.0% to 54% (Bisyarina V.P., Kazakova L.M., 1979; Babash G.V. et al., 1980; Kalinicheva V.I. et al., 1983 ; Malievsky O.A., 1994).